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Thu Dec 21 10:22:41 GMT 2006

Jason,

Great post, thanks for your knowledgable insight.

Some thoughts on what you wrote.

I rationalise the use of IV calcium chloride at time of
release on the basis of its ability to "stabilise"
myocardial cells to the resultant hyperkalaemic surge.  it
won't actually lower total body K+ concentration.  Your
thoughts on the use of resoniums prehospital however I
find interesting.  Whilst resonium will lower total body
K+, I can't see how resonium in the gastrointestinal
system is going to have much of an impact on that initial
hyperkalamic surge that will occur on crush or tourniquet
release  The resonium will take some time to bind the K+
thereby not stopping or limiting that initial
hyperkalaemic surge that will hit the heart, nor does it
provide any myocardial "stabilisation" per se.   The oral
administartion of resonium to someone who may require
urgent/immediate surgery on release concerns me, and the
ability to administer resonium PR in someone who is
trapped, crushed and requiring extrication is a mental
picture I am still battling with.

A quick look at the reference you provided for this 
comment, didn't shed any
light on resonium use prior to crush release and/or 
hospital
arrival either.

Cheers,
Stefan

Dr Stefan Mazur
Emergency Physician/Retrieval Fellow
Adelaide
Australia

On Tue, 19 Dec 2006 15:05:33 +0000
  "Jason Van der Velde" <rescue at doctors.org.uk> wrote:
> You probably knew Karim that I would eventually resist 
>no more and rise to your initial posting!!!  Time to stop 
>lurking in this fascinating tourniquet debate!!
>  
> Apologies for the lengthily reply, but particularly in 
>light of Dr. Mazur insightful comments, this is not a 
>simple topic and needs space to be addressed properly. I 
>believe I write with reasonable authority as apart from my 
>clinical work, I lecture extensively on the systemic 
>sequalea of muscle damage. It is the subject of my masters 
>thesis, and in more detail my envisaged PhD work.
>  
> 1st an observation: We are a large multidisciplinary 
>discussion group. Equally trauma is NOT the remit of only 
>one specialty or professional group. Predictably we all 
>are approaching what is essentially THE SAME kinematics 
>and pathophysiological process from different angles, 
>which is not necessary a bad thing, but may I suggest that 
>we all need to “think out of the box” that is our 
>"individual specialties". This is particularly important 
>for the patient, who’s journey is a lifetime, and not the 
>15min in the ambulance or 2 hours on the operating table. 
>Crush syndrome kills or seriously disables:
> 1)      on or shortly after extrication (Cardiac 
>Arrhythmias/thromboembolic)
> 2)      In a few days or weeks (Acute Renal 
>Failure/Cardiac Arrhythmias/thromboembolic)
> 3)      In a number of years, which as acute clinicians 
>we frequently forget! (Chronic Renal Failure)
>  
> Crush syndrome is a true systemic insult. Apart from the 
>well know renal complications of muscle damage, 
>prehospital deaths post extrication secondary to cardiac 
>arrhythmia, are frequently misdiagnosed as hypovolaemic 
>arrests and could hold a key to making a significant dent 
>in post extrication mortality statistics, ie. Peak 1 of 
>either the Scottish Trauma Audit[i] or Trunkey's[ii] 
>curve. Hence this is an important subject that requires a 
>roadside to critical care approach to management.
>  
> Electrolyte abnormalities occur frequently in patients 
>with crush-related acute renal failure.[iii] We have 
>known about such disturbances for some time now, 
>particularly the tremendous potential for hyperkalaemia 
>and consequent fatal cardiac arrhythmias.[iv] What we have 
>not fully appreciated until quite recently is the 
>staggering percentage of patients who have died either on 
>scene or en-route to hospital, as a result of electrolyte 
>abnormalities during or shortly post extrication.
>  
> Important autopsy findings from 111 deaths in the 1999 
>Athens earthquake have only recently been made public.[v] 
>Although this study’s main purpose was to audit emergency 
>response as a whole, it begins to give us the first real 
>evidence to support a long held belief of the adverse 
>effects of extrication on cardiac function. Researches 
>from the University of Athens General Hospital evaluated 
>and combined demographic data, circumstances of death, 
>rescue time, mechanisms of injury, causes of death, 
>Abbreviated Injury Scale (AIS 90) and Injury Severity 
>Score (ISS) values, vital functions and co-morbidity in a 
>study seeking to identify preventable deaths in Trunkey’s 
>first group. Their findings attributed a staggering 46.6 % 
>of post extrication earthquake deaths directly to cardiac 
>complications.
>  
> It is hypothesised that this pathophysiological process 
>is far more common than we think in every day trauma 
>practice and if this is so, it is clear that we have to 
>drastically alter our current practices, particularly our 
>prehospital practices, if we are to make any headway in 
>addressing mortality/morbidity.
>  
> Dr. Mazur has certainly presented this list with a very 
>logical approach to management. Perhaps I can add to his 
>comments by providing some additional points as well as 
>some evidence to back his management strategies up. The 
>goals are prevention and protection. There is more than 
>sufficient data to warrant an initial aggressive approach 
>to preventing fatal cardiac arrhythmias, whilst at the 
>same time initiating early, renal protective strategies. I 
>am more than happy to discuss this data further, in depth, 
>off list.
>  
> EARLY identification of at risk patients and assigning 
>them to a crush protocol is the key. Crush protocols are 
>not new. We’ve been studying them and using them since the 
>1st world war![vi] Now I can safely make the comment that 
>by the time you have biochemical diagnosis (ie. Serum CK) 
>of a crush syndrome, it is too late. The decision to 
>initiate preventative and protective strategies should be 
>a balanced, educated decision weighing up kinematics, 
>degree and time of entrapment, environmental influences 
>and premorbid health against the need for circulating 
>volume preservation and haemorrhage control.  The early 
>use of myoglobin specific urinary dipstick appears to be a 
>sensible tool in aiding such an early management 
>decision.[vii].
>  
> I believe that the key is proper training and experience 
> in identifying at risk patients by the kinematics of 
>insult alone
 How this is done is a whole discussion on 
>its own. It is also a contentious issue at the heart of 
>how we manage our prehospital emergency services. But what 
>is NOT contentious is the overwhelming evidence:
>  
> Early aggressive intervention,[viii],[ix],[x] prior to 
>extrication[xi], has been shown to benefit long term 
>outcome in entrapped casualties at risk of Crush Syndrome.
>  
> WHY prior to extrication??
> A NORMOvolaemic, NORMOtensive, NORMOthermic, NORMOetc. 
>etc. etc. system handles the “ischemic soup” that is 
>bolused from a released limb far better than one that is 
>in haemodynamic crisis... If we are going to remove a 
>crushing force or remove a tourniquet, the body has to be 
>in shape to handle it! I speak from an anaesthetic 
>perspective where I manage tourniquet release post 
>operatively on a weekly basis both electively and as an 
>emergency. Maintaining systemic normality is standard 
>perioperative management in orthopaedic, vascular, 
>plastics etc. etc. surgery. Can you all put hand on heart 
>and say you release that “ischaemic soup” into a 
>haemodynamically stable circulation each and every time?? 
>Is this why we get away with it in theatre and not in the 
>emergency room? I’m not by any means implying that each 
>and every time we take someone to theatre and put a 
>tourniquet that we don’t have a problem, of course not! 
>But it is a no-brainer that a haemodynamically stable 
>patient has a better chance...
>  
> WHY prophylactic tourniquets are good??
> There should be no ambiguity, that circulation 
>preservation strategies, i.e. permissive hypotension 
>until definitive surgical or interventional radiological 
>management of the haemorrhage, takes precedence over any 
>crush syndrome protocol. Just thought I’d make that 
>statement 1st!  I do believe in the DDIT approach with 
>tourniquets as a useful adjunct in the right circumstances 
>in haemorrhage control
 but may I add once again to the 
>argument
. WITH SYSTEMIC PREOPTIMISATION PRIOR TO RELEASE 
>!
>  
> Do you want a rescuer managing a cardiac arrhythmia 
>during the extrication? Do want to manage it in an 
>ambulance? Or do you want SOME control over when it is 
>going to occur? That is why we teach our rescue personnel 
>to put tourniquets on, prior to release and call an 
>appropriately qualified person who is able to start a 
>crush protocol to go some way to restore systemic 
>normality.
>  
> Tourniquets should remain in place until the patient is 
>in a safer environment, ideally in a hospital 
>resuscitation bay or theatre, with full cardiovascular 
>monitoring, but as a sensible compromise, in cases where 
>there is potentially a long delay to definitive care or a 
>difficult extrication, the stage release protocol could be 
>used earlier.
>  
> Once in a place of safety, with appropriate monitoring, 
>appropriate preoptimisation, a staged release of 
>tourniquets is an entirely logical next approach. This is 
>currently lacking a clinical effectiveness audit, 
>something which I aim to tackle as part of a PhD.
>  
> The goal is to do a controlled “infusion” as opposed to 
>“bolus” the inevitable ischemic washout. Tourniquets 
>should be individually released for a period of thirty 
>seconds, whilst monitoring the casualty’s condition 
>closely and then reapplied for a period of 3 minutes. 
>After reapplication, wait for 3 minutes. If the casualty 
>is stable, release the other tourniquet (if present) for 
>30 seconds. Repeat this procedure with each tourniquet 
>being released 3 times until finally being left off. 
>During this time a large CO2 and therefore acid load will 
>return to the main circulation. Ventilated patients should 
>be hyperventilated. Adverse responses can be managed with 
>further fluid, pressors, calcium and sodium bicarbonate.
>  
> To answer Dr. Mazur’s question, there is good evidence 
>in support of the early use of potassium binders such as 
>sodium polystyrene sulfonate (Sodium or Calcium Resonium) 
>orally or rectally before patients are extricated and 
>transferred to hospital.[xii] Should Calcium be used 
>prophylacticly? Well again, no evidence, but very logical. 
>I am looking into the possibility of a study in a 
>particularly earthquake prone country
 will let the list 
>know the results.  But I am about to publish one very good 
>case example where we used such agents periarrest in the 
>face of massive hyperkalaemia with discharge home 4 days 
>later!
>  
> I leave you with one thought: It can be argued that we 
> have inadvertently been efficiently managing a huge bulk 
>of patients at risk of crush syndrome through our 
>traditionally liberal approach to fluid resuscitation, 
>throughout the trauma patient journey. With today’s more 
>conservative approach to the use of fluids in trauma, 
>could we now begin to see a shift away from such problems 
>as fluid overload and ARDS to those of a crush syndrome?
> 
> Dr. Jason van der Velde       (EMDM-A, MBChB, BAA)
> Disaster Response Coordinator
> UN/OCHA Liaison
> Anaesthesia Trauma and Critical Care Team
> atacc.co.uk
> 
> [i] Jonathan Wyatt, Diana Beard, Alasdair Gray, Anthony 
>Busuttil, and Colin Robertson. The time of death after 
>trauma. BMJ 1995; 310: 1502
> [ii] Trunkey DD. Trauma. Sci Am 1983;249(2):20-7
> [iii] Sever MS, Erek E, Vanholder R, et al. The Marmara 
>earthquake: admission laboratory features of patients 
>with nephrological problems. Nephrol Dial Transplant 
>2002;17:1025-1031.
> [iv] James PB. Cardiac arrest after crush injury. Br Med 
>J (Clin Res Ed). 1983 Sep 17;287(6395):839.
> [v] Papadopoulos IN, Kanakaris N, Triantafillidis A, et. 
>al.  Autopsy findings from 111 deaths in the 1999 Athens 
>earthquake as a basis for auditing the emergency response. 
>Br J Surg. 2004 Dec;91(12):1633-40
> [vi] Frankenthal L. Lieber Verschuettungen. Virchows 
>Archives 1916;22:332-45 (in German).
> [vii] Apple, F.S., Y. Hellsten, and P.M. Clarkson. Early 
>detection of skeletal muscle injury by assay of creatine 
>kinase MM isoforms in serum after acute exercise. Clin. 
>Chem. 34(6): 1102-1104, 1988.
> [viii] Better OS. The crush syndrome revisited 
>(1940-1990). Nephron 1990;55:97-103.
> [ix] Better OS, Rubinstein I, Reis ND. Muscle crush 
>compartment syndrome: fulminant local oedema with 
>threatening systemic effects. Kid Int 2003;63:1155-7.
> [x] Malinoski DJ, Slater MS, Mullins RJ. Crush injury 
>and rhabdomyolysis. Crit Care Clin. 2004 Jan;20(1):171-92
> [xi] Gunal AI, Celiker H, Dogukan A, et. al. Early and 
>vigorous fluid resuscitation prevents acute renal failure 
>in the crush victims of catastrophic earthquakes.  J Am 
>Soc Nephrol. 2004 Jul;15(7):1862-7
> [xii] Sever MS, Vanholder R, Lameire N. Management of 
>crush-related injuries after disasters. N Engl J Med. 
>2006 Mar 9;354(10):1052-63.
> 
> 
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